Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes

A. E. Butler, R. P. Robertson, R. Hernandez, A. V. Matveyenko, T. Gurlo, P. C. Butler

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

Aims/hypothesis The beta cell transcriptional factor musculoaponeurotic fibrosarcoma oncogene family A (MafA) regulates genes important for beta cell function. Loss of nuclear MafA has been implicated in beta cell dysfunction in animal models of type 2 diabetes. We sought to establish if nuclear MafA is less abundant in beta cell nuclei in humans with type 2 diabetes. Methods Pancreas obtained at surgery from five nondiabetic individuals and six individuals with type 2 diabetes was immunostained for insulin, glucagon and MafA. Results Beta cell nuclear MafA was markedly decreased in type 2 diabetes (1.6±1.2% vs 46.3±8.3%, p<0.001). Conclusions/interpretation Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.

Original languageEnglish (US)
Pages (from-to)2985-2988
Number of pages4
JournalDiabetologia
Volume55
Issue number11
DOIs
StatePublished - Nov 2012

Keywords

  • Beta cell
  • Glucotoxicity
  • MafA

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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